Alkali poisoning is a pathological condition caused by ingestion of caustic soda, concentrated ammonia, potash, caustic soda. In rare cases, inhalation forms of the lesion are noted. Symptoms include traces of chemical burns in and around the mouth, severe pain, swelling of the upper respiratory tract and esophagus, shock. Pathology is diagnosed on the basis of anamnesis and the results of fibrogastroscopy. Auxiliary methods — clinical and biochemical blood analysis, if necessary — CT, MRI. Specific treatment involves analgesia, the appointment of hemostatic, antibacterial, regenerating agents, gastric lavage.
T54.3 Toxic effect of caustic alkalis and alkali-like substances
Alkaline burns account for about 15-20% of the total number of poisoning with cauterizing poisons. The most common lesions caused by ingestion of ammonia. The mortality rate is about 5%, the lethal dose of 10% ammonia is 50-100 ml. At the end of the XIX century, most of these poisonings were caused by caustic soda, which was widely used as a hygiene product. Almost half of the patients died, the rest became deeply disabled. Today, such cases are not very common, because the substance has gone out of use. Alkali poisoning caused by new detergents, the hydrogen index of which is close to 10, is more common.
A common cause of injury is accidental ingestion of a toxicant. This is possible when storing toxic substances in food containers in places where food is usually located (refrigerator, cellar). Risk group: young children, alcohol-dependent persons in a state of abstinence, mentally unhealthy family members. Especially often there are lesions with a means to combat blockages “MOLE”, ammonia, caustic soda. Other possible reasons:
- Attempts to sober up. A common folk way to quickly sober up after drinking alcohol is the use of a few drops of ammonia in a glass of water. When using excessively concentrated solutions, traumatization of the tissues of the gastrointestinal tract is possible.
- Suicide. Attempts at self-retirement account for no more than 0.5% of the total number of cases. Alkali poisoning as a method of suicide is rarely chosen, while patients try to drink the maximum possible amount of poison. Their burns have a large area and depth.
- Industrial accidents. When alkaline compounds are released into the air of an industrial zone, inhalation poisoning of workers occurs mainly. There is a lesion of the respiratory tract, external mucous membranes. The mortality rate is relatively low. The main cause of death is toxic pulmonary edema, respiratory failure.
When alkalis come into contact with living tissues, hydroxide ions are formed, which have a destructive effect. Fats are saponified, protein substrates of cells are dissolved, albuminates are synthesized. The formation of a scab that prevents further penetration of the poison does not occur. Alkali poisoning is characterized by a deeper lesion compared to acid burns. The esophagus mainly suffers. The acid contained in the stomach has a neutralizing effect and prevents the occurrence of injury.
After absorption, the salts formed as a result of the transformation of the alkaline component become the cause of alkalosis. Neuromuscular excitability increases, convulsive readiness appears. Insoluble phosphates are synthesized, which leads to a decrease in the concentration of ionized calcium. Cerebral and coronary blood flow worsens, hemodynamic disorders occur. In the future, symptoms develop caused by the toxic effect of products formed as a result of the cleavage of necrotic tissues.
Alkali poisoning is divided by the type of agent (ammonia, caustic soda, caustic soda), severity (mild, severe, moderate severity), localization of injury (predominant damage to the oral cavity, esophagus, respiratory tract), stage (toxicogenic, somatogenic). Division by the presence of complications (complicated by perforation, infection, shock) is also used. The most common classification parameter is considered to be the depth of the burn:
- I degree. Damage to the surface layers of the epithelium of the mucous membrane of the oral cavity and esophagus. It has no serious consequences, it recovers without the formation of strictures and scarring. Occurs when using a small amount of a toxicant with a low concentration.
- II degree. Characterized by extensive necrosis of the epithelium, the process affects the mucous membrane throughout its thickness. It is not accompanied by long-term consequences, but requires a longer time to recover. Occurs in situations where the period of contact with the poison does not exceed 30-60 seconds (quickly rendered assistance).
- III degree. Not only the mucous membrane is involved, but also the muscular layers of the organ. With severe injuries, there is a lesion of paraesophageal fiber, nearby organs. Usually accompanied by the development of shock, significant systemic disorders. Subsequently, it leads to the formation of post-traumatic stenosis. It occurs in suicidal attempts and accidental use of a large volume of a toxicant.
Poisoning is manifested by a sharp pain in the mouth, behind the sternum immediately after taking the poison. The patient is scared, rushes. There is psychomotor agitation caused by fear and severe pain syndrome. Sometimes vomiting develops after injury. There is an increase in salivation, salivation. After 30-60 minutes, signs of oedema of the esophagus appear: difficult and painful swallowing, a feeling of pressure. There is no scab on the lips and chin, characteristic of acid damage.
Injuries corresponding to the III degree of severity are often accompanied by shock. In the erectile phase, the victim shows unhealthy activity, does not realize the danger of the injuries received. In torpid there is depression of consciousness, weakening of hemodynamics, centralization of blood circulation. The skin is pale or marbled, blood pressure is sharply reduced, independent breathing is preserved or disturbed. Compensatory tachycardia is determined, which is replaced by bradycardia.
Poisoning with inhalation-type alkalis leads to increased lacrimation, hyperemia of the conjunctiva of the eyes. The patient develops a cough that acquires a barking character with laryngeal edema. A significant narrowing of the lumen of the URT causes respiratory insufficiency of a mechanical type: difficulty in inhaling and exhaling, diffuse cyanosis, inclusion in the work of auxiliary respiratory muscles, nose wings. Against the background of pulmonary edema, wet wheezing and foaming from the mouth are added to the clinical picture.
The main complication of chemical burns is perforation of the esophagus with the development of mediastinitis. It occurs in 1-2% of patients at the stage of splitting necrotic masses and in 0.4-0.5% of victims who underwent FGDS procedure. It is characterized by the formation of emphysema, the appearance of blood in vomit, increased soreness. With the purulent nature of the process, there are signs of a general toxic syndrome: hyperthermia, general deterioration of well-being, aches and pain in the muscles, increased ESR, leukocytosis. It is impossible to exclude the development of infectious and toxic shock.
Another common complication is bleeding. It is detected mainly at the stage of healing of burns, in violation of the recommended diet. It is observed with injuries of the III degree. Delayed consequence, diagnosed in 40-50% of patients who have suffered massive chemical lesions — esophageal strictures. They form after 0.5-2 years, accompanied by complete or partial obstruction of the organ. There is evidence of scar malignancy, but such cases are rare.
Poisoning with alkalis at the prehospital stage is established by the ambulance team. After arriving at the hospital, the diagnosis is confirmed by a toxicologist with the involvement of endoscopists and a consultant surgeon. Differential diagnosis is made with poisoning by other cauterizing substances, mainly acids. The following examinations are required:
- Physical. It is realized at the first contact with the patient and at his admission to the hospital. Characteristic clinical signs of the lesion are detected. Blood pressure is above 140/90, with shock — less than 80/50 mm Hg. The heart rate is 90-120 beats / minute. The patient is scared, there is a fussiness of behavior.
- Hardware. The main method is FGDS. Signs of tissue melting, edema, hyperemia, zones of fibrinoid necrosis, ulceration are detected in the esophagus. The places of physiological constrictions are most affected. With massive deep burns, the study is difficult. The X-ray may show signs of organ rupture.
- Blood test. The study of ABB indicates a drop in the plasma calcium content below 2 mmol/l, a shift in the oxygen index towards alkalosis. A general blood test allows you to determine non—specific signs of inflammation – leukocytosis, ESR growth. In the later stages, an increase in creatinine and urea levels is possible. In the coagulogram, changes characteristic of the DIC syndrome are detected.
Before the arrival of the ambulance team, it is forbidden to cause vomiting in the victim – this increases the depth of burns and increases the risk of perforation. Activated charcoal should not be given, since alkalis are not sorbed on it, and the passage of solid tablets through the esophagus contributes to its additional traumatization. It is necessary to give the patient a semi-sitting position, calm him down, give him unboiled milk or protein water to drink. It is not recommended to completely lay the patient, as this contributes to the development of esophageal reflux.
Gastric lavage is performed through a probe, pure water or a mixture consisting of 50% water and a similar amount of milk is used. Before insertion, the catheter must be liberally lubricated with sterile vaseline. After the procedure, vegetable oil is injected into the stomach, which promotes the transformation of alkali into soap. This should be done naturally so that the substance passes through the esophagus, softening it and neutralizing the toxin. Before starting the procedure, analgesia with the use of narcotic drugs is indicated.
To prevent early bleeding, an infusion of hemostatic agents is allowed. Pronounced pharyngeal edema is an indication for intravenous administration of glucocorticosteroids or local irrigation of tissues with them. In cases of shock, adrenaline, dopamine, artificial respiratory support, and hardware monitoring are used. Hospitalization in the general department is carried out with moderate and light injuries, in intensive care — with a significant violation of vital functions.
Alkali poisoning requires hemostatic, anti-inflammatory, analgesic and antitoxic therapy. In order to prevent infectious complications, antibiotics are used. Forced diuresis is used to remove toxins. If necessary, hepatoprotective agents, antispasmodics, anticoagulants, hormones are prescribed. The patient must follow a diet.
Surgical correction is carried out at the acute stage of the disease if the patient has signs of esophageal perforation. In addition, hemostasis can be performed surgically. As a rule, endoscopic access is used. The necessary area is pricked with vasoconstrictors or cauterized with silver nitrate. A few years after discharge, the patient may need plastic surgery of the esophagus due to partial obstruction of the organ due to strictures.
Prognosis and prevention
In case of alkali poisoning, which caused burns of I-II degree, the prognosis for life is favorable. The mucous membrane usually recovers completely, the average hospital stay is 21 days. Severe injuries in 27% of cases are accompanied by severe systemic disorders, multiple organ failure. Even with timely and competent first aid, the mortality rate exceeds 25-30%. If more than 1-2 hours have passed from the moment of the incident to the start of therapeutic measures, the mortality rate increases to 35-40%.
To prevent poisoning with alkalis, it is necessary to abandon the storage of these substances together with food. It is recommended to keep household chemicals in factory containers, under lock and key, without access for children, the elderly, dementia sufferers, persons with an unbalanced psyche. At work, workers in contact with toxic substances are required to use personal respiratory protection equipment: respirators, gas masks.